PHYSIOLOGICAL

INTEGRITY: ACUTE
BIOLOGIC CRISIS
Irene Shara L. Castillon

RESPONSES TO ALTERED

RESPIRATORY
FUNCTION

RESPIRATORY FAILURE

Failure in Gas exchange due to either

pump of heart or Lung failure or both.
Condition in which the lungs fail to
oxygenate the blood adequately and
prevent carbon dioxide retention

 Ventilation

the air that reaches the

alveoli
Perfusion the blood that reaches
the alveoli

MECHANISMS LEADING TO
RESPIRATORY FAILURE

Characterized by:
Hypoxemic Respiratory Failure
O2, N- CO2, Metabolic Acidosis
Hypercapnic Respiratory Failure
02, CO2, Respiratory Acidosis
Major manifestation of Respiratory Failure are
Hypoxemia and Hypercapnia or both

Mechanism that can lead to

Respiratory Failure
Impaired Ventilation
occurs when the volume of the fresh air moving
into and out of the lungs is significantly reduced.
Impaired Diffusion
Restricted transfer of oxygen and/or carbon
dioxide across the alveolar capillary junction

Impaired Matching
of Ventilation and
Perfusion

v/Q Perfusion without

ventilation is a blocked
airway.
V/q Ventilation without
perfusion is a blocked
capillary

MANAGEMENT
Mechanical Ventilation (Negative pressure,
Positive pressure)
Endotracheal Intubation
Oxygen Therapy

ACUTE RESPIRATORY
DISTRESS SYNDROME

Cause by diffuse lung injury and leads to

extravascular lung fluid, specifically in the
alveolar capillary membrane.

Initial Manifestation of ARDS typically

develop 24-48 hours after the initial insult
Manifestation:

Tachypnea
Dyspnea
Deteriorating ABG levels ( 02, even with 02
delivery)
Lung Compliance
Use of Accessory Muscles

MANAGEMENT

Treat the cause

O2 therapy
Fowlers position
Fluid intake Restriction
Administer Diuretics, Anticoagulants or
Corticosteroids
Intubation or mechanical ventilator using PEEP

CHRONIC OBSTRUCTIVE
PULMONARY DISEASE

Slowly progressive obstruction of the airways

Characterized by:
EMPHYSEMA Pink Puffer
It compensates by hyperventilation.
Less hypoxemia
CHRONIC BRONCHITIS Blue Bloater
Hypoxemia is worst.

MANAGEMENT
Monitor VS, Pulse Oximetry
Administer low concentration of Oxygen (12L/min)
Instruct in Abdominal Breathing and pursed-lip
breathing techniques
Place the client in fowlers position and leaning
forward
Administer Bronchodilators and Corticosteroids
High protein, High Calorie intake

RESPONSES TO ALTERED

NUTRITION AND
METABOLISM
FUNCTION

LIVER CIRRHOSIS
Diffuse degeneration of the liver and
destruction of hepatocytes
Types
o Laennecs Cirrhosis
o Post-Necrotic Cirrhosis
o Biliary Cirrhosis
o Cardiac Cirrhosis

COMPLICATIONS
Portal Hypertension
Ascites
Bleeding Esophageal Varices
Coagulation defects
Jaundice
Portal Systemic Encelophathy
Hepatorenal Syndrome

MANAGEMENT

Weight and Check Abdominal Girth Daily.

Fowlers Position
Provide Supplemental Vitamins (B-complex,
Vitamins A, C and K, Folic acid and thiamine)
Restrict H20 and NA
Monitor for Asterixis and Fector Hepaticus
Gastric Intubation or Balloon Tamponade for
Esophageal Varices
Monitor Coagulation Therapy
Meds: Diuretics, Lactulose, Oxazepam
Paracentesis

DIABETIC KETOACIDOSIS
Sudden onset
Occurs in people with Type 1 DM
Precipitating Factors
Inadequate Insulin dose/Infection
Characterized by:

blood glucose

serum pH
ketonuria

Manifestation
Dehydration (dry mucus membranes,
tachycardia, hypotension)
Fruity odor to breath: Acetone
Acidosis: Kussmaul breathing, change in
consciousness
Signs of infection: fever, oropharyngeal
erythema, boils on skin
Electrolyte Loss

Management

Fluid Replacement
Insulin Administration
Electrolyte Imbalance correction

NON-KETOTIC
HYPERGLYCEMIC
HYPERSOMOLAR SYNDROME

Onset is gradual
Occurs in people with type 2 DM
Precipitating Factors
Poor fluid intake or infection
Characterized by:
Plasma

Osmolarity >340 mOsm/L

Greatly elevated blood glucose (>600mg/dL)
Altered LOC

Management
Fluid Replacement
Insulin Administration
Electrolyte Imbalance correction

Responses to Altered

ELIMINATION
FUNCTION

ACUTE RENAL FAILURE

Reversible

Characterized by accumulation of
nitrogenous wastes in the blood and
alterations in body fluids

Has 3 Causes
PRERENAL FAILURE
Conditions affecting before reaching the
nephrons
INTRARENAL FAILURE
Conditions affecting nephron itself.
POSTRENAL FAILURE
Conditions affecting beyond the nephron or the
urinary tract.
Obstruction of the urine collecting system

3 STAGES OF ARF
Oliguric/Anuric Phase
lasts between 8-14 days
Great reduction in the GFR
Increased BUN/Creatinine
Electrolyte abnormalities (hyperkalemia,
hyperphosphatemia and hypocalcemia)
Metabolic acidosis

Diuretic Phase
source of obstruction has been removed but
the residual scarring and edema of the renal
tubules remains
last 7-14 days and is characterized by:
Increase in glomerular filtration rate (GFR)
Urine output as high as 2-4 L/day
Urine that flows through renal tubules
Renal cells that cannot concentrate urine

Recovery Period Phase

last from several months to over a year
Condition is getting back to normal function
(if damage was significant, BUN and
Creatinine may never return to normal
levels)
GFR has usually returned to 70% to 80% of
normal.

Diagnostic Test

Urinalysis
Serum Creatinine and BUN
Serum Electrolytes
ABG
CBC
Renal Ultrasonography
CT- Scan
Intravenous Pyelography
Renal Biopsy

Management
Fluid Restriction
Dietary Management
Medication Administration
Diuretic (Loop and Osmotic Diuretic)
Electrolyte Replacement (Calcium,
Potassium)
Erythropoietin
Dialysis

CHRONIC RENAL FAILURE

Progressive irreversible kidney injury.

When kidney function is too poor to sustain
life, CRF is termed End-stage renal disease
80% of nephrons stop working before
symptoms show up, a silent disease

Manifestation
Uremic Frost
Uremia
Anemia
Hypertension
Uremic Fretor (Urine-like breath)
Renal Encepalophathy
CNS Manifestation

Stage 1: Reduced Renal Reserve

a 40-75% loss of nephron function, no
symptoms
Polyuria/ Nocturia- First sign of CHF. From
the loss of nephron functioning and
kidneys can not concentrate the urine

Stage 2: Renal Insufficiency

78-80% nephron function is lost and
replaced by scare tissue. Symptoms begin
CLINICAL SIGN: Hyponatremia, increased
BUN and Creatinine.

Stage 3: Final Stage

End Stage Renal Disease ESRD only 10% of
nephrons remain functioning

Management
Fluid Regulation
Dietary Management
Skin Care
Potassium and Phosphorous restriction
Medications
Diuretics
Electrolyte Imbalances Corrections
Insulin Administration
Folic Acid/Ferrous Sulfate

LONG-TERM MANAGEMENT
Dialysis
Kidney Transplant

Reference

Ignatavicius D. and Workman, M. (2006) Medical-surgical nursing

(Fifth edition). United states of America: Elsevier saunders

Porth, C. (2005) Pathophysiology (seventh edition). Philadelphia:

Lippincott Williams and Wilkins

Lemone, P. and Burke, K. (2004) Medical surgical nursing (third

edition). New Jersey: Pearson Education, Inc.